Increases in insulin signaling following electrical pulse stimulation are blunted in myotubes derived from severely obese individuals with or without type 2 diabetes

Type 2 diabetes mellitus is a progressive disease that is characterized by the appearance of insulin resistance. The term insulin resistance is very wide and could affect different proteins involved in insulin signaling, as well as other mechanisms. In this review, we have analyzed the main molecular mechanisms that could be involved in the connection between type 2 diabetes and neurodegeneration, in general, and more specifically with the appearance of Alzheimer’s disease. We have studied, in more detail, the different processes involved, such as inflammation, endoplasmic reticulum stress, autophagy, and mitochondrial dysfunction.

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Effects of Metformin and Rosiglitazone Treatment on Insulin Signaling and Glucose Uptake in Patients With Newly Diagnosed Type 2 Diabetes: A Randomized Controlled Study

Diabetes ◽

10.2337/diabetes.54.5.1459 ◽

2005 ◽

Vol 54 (5) ◽

pp. 1459-1467 ◽

Cited By ~ 66

Author(s):

H. K.R. Karlsson ◽

K. Hallsten ◽

M. Bjornholm ◽

H. Tsuchida ◽

A. V. Chibalin ◽

...

Keyword(s):

Type 2 Diabetes ◽

Glucose Uptake ◽

Insulin Signaling ◽

Randomized Controlled Study ◽

Controlled Study ◽

Newly Diagnosed ◽

Randomized Controlled ◽

Rosiglitazone Treatment

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Comprehensive Review on Neuro-Degenerative Type 3DM

Current Diabetes Reviews ◽

10.2174/1573399818666211213103624 ◽

2021 ◽

Vol 18 ◽

Author(s):

Chandani V. Chandarana ◽

Salona Roy

Keyword(s):

Type 2 Diabetes ◽

Insulin Signaling ◽

Insulin Signalling ◽

Amyloid Β ◽

Diabetes Mellitus Type 1 ◽

Current Data ◽

The Body ◽

Type I ◽

Therapeutic Benefits

: Alzheimer disease (AD) is thought to be the metabolic illness raised by defective insulin signaling, insulin resistance, and low insulin levels in the brain, according to a growing body of research. The "Type 3 diabetes" has been postulated for AD because reduced insulin signalling has molecular and physiological consequences that are comparable to Type I and Type 2 diabetes mellitus (Type 1 DM and Type 2 DM, respectively). The similarities between type 2 diabetes and Alzheimer's disease suggest that these clinical trials might yield therapeutic benefits. However, it's important to note that lowering your risk of Alzheimer's dementia, whether you have diabetes or not, is still a multidimensional process involving factors like exercise, smoking, alcohol, food, and mental challenge. The current aim is to show the relationship between T3D and AD being based on both the processing of amyloid-β (Aβ) precursor protein toxicity and the clearance of Aβ are the result of an impaired insulin signaling. The brain's metabolism with its high lipid content and energy needs, places excess demands on mitochondria and appears more susceptible to oxidative damage than the rest of the body. Current data suggests that increased oxidative stress relates to amyloid-β (Aβ) pathology and onset of AD.

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Electrical Pulse Stimulation of Primary Human Skeletal Muscle Cells

Methods in Molecular Biology - Myogenesis ◽

10.1007/978-1-4939-8897-6_2 ◽

2018 ◽

pp. 17-24 ◽

Cited By ~ 4

Author(s):

Nataša Nikolić ◽

Vigdis Aas

Keyword(s):

Skeletal Muscle ◽

Human Skeletal Muscle ◽

Muscle Cells ◽

Skeletal Muscle Cells ◽

Electrical Pulse ◽

Electrical Pulse Stimulation ◽

Human Skeletal Muscle Cells ◽

Pulse Stimulation ◽

Stimulation Of

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Transcriptome Analyses of In Vitro Exercise Models by Clenbuterol Supplementation or Electrical Pulse Stimulation

Applied Sciences ◽

10.3390/app112110436 ◽

2021 ◽

Vol 11 (21) ◽

pp. 10436

Author(s):

Taku Fukushima ◽

Miho Takata ◽

Ayano Kato ◽

Takayuki Uchida ◽

Takeshi Nikawa ◽

...

Keyword(s):

Gene Ontology ◽

Electrical Pulse ◽

C2c12 Myotubes ◽

Rna Seq ◽

Gene Expressions ◽

Beneficial Effects ◽

Electrical Pulse Stimulation ◽

Transcriptional Changes ◽

Pulse Stimulation

Exercise has beneficial effects on human health and is affected by two different pathways; motoneuron and endocrine. For the advancement of exercise research, in vitro exercise models are essential. We established two in vitro exercise models using C2C12 myotubes; EPS (electrical pulse stimulation) for a motoneuron model and clenbuterol, a specific β2 adrenergic receptor agonist, treatment for an endocrine model. For clenbuterol treatment, we found that Ppargc1a was induced only in low glucose media (1 mg/mL) using a 1-h treatment of 30 ng/mL clenbuterol. Global transcriptional changes of clenbuterol treatment were analyzed by RNA-seq and gene ontology analyses and indicated that mitogenesis and the PI3K-Akt pathway were enhanced, which is consistent with the effects of exercise. Cxcl1 and Cxcl5 were identified as candidate myokines induced by adrenaline. As for the EPS model, we compared 1 Hz of 1-pulse EPS and 1 Hz of 10-pulse EPS for 24 h and determined Myh gene expressions. Ten-pulse EPS induced higher Myh2 and Myh7 expression. Global transcriptional changes of 10-pulse EPS were also analyzed using RNA-seq, and gene ontology analyses indicated that CaMK signaling and hypertrophy pathways were enhanced, which is also consistent with the effects of exercise. In this paper, we provided two transcriptome results of in vitro exercise models and these databases will contribute to advances in exercise research.

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Effect of differentiation, de novo innervation, and electrical pulse stimulation on mRNA and protein expression of Na+,K+-ATPase, FXYD1, and FXYD5 in cultured human skeletal muscle cells

PLoS ONE ◽

10.1371/journal.pone.0247377 ◽

2021 ◽

Vol 16 (2) ◽

pp. e0247377

Author(s):

Vid Jan ◽

Katarina Miš ◽

Natasa Nikolic ◽

Klemen Dolinar ◽

Metka Petrič ◽

...

Keyword(s):

Skeletal Muscle ◽

Mrna Expression ◽

Human Skeletal Muscle ◽

De Novo ◽

Muscle Cells ◽

Electrical Pulse ◽

Electrical Pulse Stimulation ◽

Human Skeletal Muscle Cells ◽

Pulse Stimulation ◽

Low Serum

Denervation reduces the abundance of Na+,K+-ATPase (NKA) in skeletal muscle, while reinnervation increases it. Primary human skeletal muscle cells, the most widely used model to study human skeletal muscle in vitro, are usually cultured as myoblasts or myotubes without neurons and typically do not contract spontaneously, which might affect their ability to express and regulate NKA. We determined how differentiation, de novo innervation, and electrical pulse stimulation affect expression of NKA (α and β) subunits and NKA regulators FXYD1 (phospholemman) and FXYD5 (dysadherin). Differentiation of myoblasts into myotubes under low serum conditions increased expression of myogenic markers CD56 (NCAM1), desmin, myosin heavy chains, dihydropyridine receptor subunit α1S, and SERCA2 as well as NKAα2 and FXYD1, while it decreased expression of FXYD5 mRNA. Myotubes, which were innervated de novo by motor neurons in co-culture with the embryonic rat spinal cord explants, started to contract spontaneously within 7–10 days. A short-term co-culture (10–11 days) promoted mRNA expression of myokines, such as IL-6, IL-7, IL-8, and IL-15, but did not affect mRNA expression of NKA, FXYDs, or myokines, such as musclin, cathepsin B, meteorin-like protein, or SPARC. A long-term co-culture (21 days) increased the protein abundance of NKAα1, NKAα2, FXYD1, and phospho-FXYD1Ser68 without attendant changes in mRNA levels. Suppression of neuromuscular transmission with α-bungarotoxin or tubocurarine for 24 h did not alter NKA or FXYD mRNA expression. Electrical pulse stimulation (48 h) of non-innervated myotubes promoted mRNA expression of NKAβ2, NKAβ3, FXYD1, and FXYD5. In conclusion, low serum concentration promotes NKAα2 and FXYD1 expression, while de novo innervation is not essential for upregulation of NKAα2 and FXYD1 mRNA in cultured myotubes. Finally, although innervation and EPS both stimulate contractions of myotubes, they exert distinct effects on the expression of NKA and FXYDs.

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